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2相折返是触发于心肌动作电位时程2相吗? 被引量:4

Does phase 2 reentry really be triggered in phase 2 of action potential duration in myocardium?
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摘要 2相折返被认为是在特定的条件下,心室肌动作电位时程差异过大,毗邻细胞分别处于高电位2相和可兴奋间期,显著的电压梯度引起较强的电紧张性扩布,导致折返发生。但心脏异质性本身是相对宏观的概念,相邻细胞间心肌异质性并不明显,其动作电位时程的差异也不可能过大,邻近细胞间能否激动既取决于细胞跨壁电压差,也取决于心肌细胞离子通道即时功能状态。而心室肌动作电位时程3相变化幅度大,且存在超常期,易于激动,相邻细胞间较短的动作电位时程差异即为心律失常的发生提供了可能。因此,2相折返触发高电位可能更多在于心室肌动作电位3相,而非2相。 Phase 2 reentry is considered to happen in phase 2 of action potential duration in myocardium when the adjacent ventricular cells are respectively in a high potential state and excitable period so that the high voltage gradient leads to stronger electrotonie spread. However, the heterogeneity of the heart is a relative concept macroscopically. Microscopically, the heterogeneity between the adjacent cells is not obvious, and the difference in the action potential duration is not remarkable. Whether the myocardial cells can be excited or not depends on both the voltage difference among the cytomembranes and the real-time function state of ion channels. As for the phase 3 of action potential duration in myocardium, large varied amplitude of voltage gradient happens in this period, and it includes supernormal phase, which makes myocardial cells excited easily. In the phase 3, the minor differences in the action potential duration between adjacent cells can offer the conditions for arrhythmia development. Therefore, the phase 2 reentry is triggered by high potential in phase 3 of action potential duration in myocardium rather than in phase 2.
出处 《医学争鸣》 北大核心 2017年第4期51-54,共4页 Negative
关键词 2相折返 心律失常 室性 心室肌3相 动作电位时程 phase 2 reentry arrhythmia, ventricular action potential phase 3 ofventricular muscle action potential duration
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  • 1严干新,姚青海,王东琦,崔长琮.J波与J波综合征[J].中华心律失常学杂志,2004,8(6):360-365. 被引量:67
  • 2王劲风,单其俊,杨兵,陈明龙,邹建刚,陈椿,徐东杰,曹克将.T 波峰-末间期与Brugada综合征危险分层的相关性研究[J].中华心血管病杂志,2007,35(7):629-632. 被引量:8
  • 3Ball J, Carrington M J, MeMurray J J, el al. Atrial fibrillation: profile and burden of an ewdving epidemic in the 21st tenths,, lnt J Cardiol, 2013, 167: 1807-1824.
  • 4He XZ, Wang HY. Shen Y. el al. Cardiomyocyte progenitors in a canine pulmonary vein model of persistent atrial fibrillalion. J Cardiol, 2012, 60: 242-247.
  • 5Namekala I, Tsuneoka Y, Tanaka H. Eleclrophysiological and pharmacological properties of the pulmonary vein myocardinm. Biol Pharm Bull, 2013, 36: 2-7.
  • 6Harem S. Biology of the substrata of alrial fibrillation. Biol Aujourdhui, 2012, 206: 5-9.
  • 7Xu Y, Sharma D, Li G, et al, Atrial remodeling: New pathopiaysiological mechanism if atrial fihrillation. Med Hypolheses, 2013, 80: 53-56.
  • 8Sasaki N, Okumura Y. Watanabe I, et al. Pulmonary vein remnant as a trigger site for atrial fibrillalinn. Circ J, 2013, 77: 494-496.
  • 9Medi C, Kalman JM, Ling LH, et al. Atrial electrical and structural remodeling associated with longstanding pulmonary hypertension and right ventricular hypertrophy in humans. J Cardiovasc Electrophysiol, 2012, 23: 614-620.
  • 10Sossalla S. Kallmeyer B. Wagner S, et al. Altered Na+ eurrents in atrial fibrillation effects of ranolazine on arrhythmias and contractility in human atrial myocardium. J Am Coil Cardiol. 2010, 55: 2330-2342.

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